56
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      The role of oxidative stress in noise-induced hearing loss.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Modern research has provided new insights into the biological mechanisms of noise-induced hearing loss, and with these new insights comes hope for possible prevention or treatment. Underlying the classic set of cochlear pathologies that occur as a result of noise exposure are increased levels of reactive oxygen species (ROS) that play a significant role in noise-induced hair cell death. Both necrotic and apoptotic cell death have been identified in the cochlea. Included in the current review is a brief review of ROS, along with a description of sources of cochlear ROS generation and how ROS can damage cochlear tissue. The pathways of necrotic and apoptotic cell death are also reviewed. Interventions are discussed that target the prevention of noise-induced hair cell death: the use of antioxidants to scavenge and eliminate the damaging ROS, pharmacological interventions to limit the damage resulting from ROS, and new techniques aimed at interrupting the apoptotic biochemical cascade that results in the death of irreplaceable hair cells.

          Related collections

          Author and article information

          Journal
          Ear Hear
          Ear and hearing
          Ovid Technologies (Wolters Kluwer Health)
          0196-0202
          0196-0202
          Feb 2006
          : 27
          : 1
          Affiliations
          [1 ] Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, Buffalo, New York 14214, USA. donaldhe@buffalo.edu
          Article
          00003446-200602000-00001
          10.1097/01.aud.0000191942.36672.f3
          16446561
          1e113cad-0fc9-40b8-8ecc-2874f38531ef
          History

          Comments

          Comment on this article